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Motor Sequela of Dementia, Devi 1 Motor Sequela of Dementia Gayatri Devi, MD Motor Disorders, 2nd Edition by David S. Younger, MD, Editor. Lippincott Williams & Wilkins, Philadelphia © 2005. Address for correspondence: The NY Memory and Healthy Aging Services 65 East 76th Street New York, NY 10021-1844 Tel: (212) 517 6881 Fax: (212) 517 6921 Motor Sequela of Dementia, Devi 2 Introduction: Consideration of motor disorders in patients with dementia is of clinical importance in establishing the etiopathogenesis of dementia in affected patients, and in many instances, in determining disease progression and prognosis. The motor manifestations may vary from mild extrapyramidal rigidity to paralysis depending on the type and the stage of the dementia. For example, patients with Alzheimer disease (AD) develop parkinsonian features and motor difficulties later in their illness; such symptoms at onset should prompt consideration of dementia due to Lewy bodies (DLB) or another type of dementia1,2. An alternative reason would be a more aggressive type of AD, often associated with a worse prognosis3,4. This chapter addresses motor disorders early and late in the course of dementia of various causes along with the epidemiology, pathophysiology and available treatments. The dementias associated with acquired immunodeficiency syndrome, normal pressure hydrocephalus, and motor neuron diseases are covered elsewhere. Alzheimer Disease: While the pathology is identical, AD can be divided into two clinically different phenotypes defined by different genotypes, namely early onset AD (EOAD), with age at onset prior to the age of 60, and late onset AD (LOAD), with an onset after 60 to 65 years5,6. About 5% of cases of AD are of the EOAD type. Autosomal dominant mutations in the presenilin 1 gene on chromosome 14 (the most common type), in the presenilin 2 gene on chromosome 1 or the APP gene on chromosome 21, as seen in patients with trisomy 21, account for about half of the cases of EOAD5,6. Patients with EOAD typically manifest myoclonus, parkinsonism, and psychiatric features early in their course with rapid progression to infirmity and death7,8. They may be misdiagnosed by virtue of their relative youth. Motor Sequela of Dementia, Devi 3 In one kindred9, the proband developed depression at 29 followed by dementia one year afterward, and dysarthria, aphasia and myoclonus four years later. He developed seizures by age 36 and died at 38. His brother developed cognitive impairment at age 27, and by 30 had aphasia, myoclonus and generalized seizures, followed by limb rigidity at 32 and death a year later. The father had mood swings from age 35 followed by violent temper, dementia, generalized seizures and myoclonus from age 38. A clinical diagnosis of Creutzfeld-Jakob disease was made, although brain pathology subsequently revealed AD. This family, with an exceptionally early age of onset and a virulent course characterized by early motor disturbances, was found to have a mutation in the PS1 gene on chromosome 149. The molecular pathogenesis of EOAD reflects acceleration of abnormal accumulation of beta amyloid and tau protein. Genetic screens are commercially available to screen for the commonest mutations. However, as it appears that many families have a ‘private’ mutation unique to that family, a negative genetic screen for common mutations for EOAD does not preclude the diagnosis10. While the response to treatment in EOAD has been less well studied than late onset AD, treatment with acetylcholinesterase inhibitors and N-methyl D-aspartate (NMDA) antagonists such as memantine is warranted. The course of LOAD is more indolent than that of EOAD, with a prevalence of 9% above the age of 65, rising to between 35% and 50% in persons above the age of 8511,12. Women are at a higher risk than men even after controlling for greater longevity, although this issue is controversial13. In contrast to EOAD, LOAD manifests a multi-factorial etiology with contributions from genetics and the environment14,15. The presence of the E4 isoform of the apolipoprotien E gene on chromosome 19, as well as alpha-2-macroglobulin polymorphisms significantly increases the risk for the disorder16. Other associations with variants in the sortilin- Motor Sequela of Dementia, Devi 4 related receptor 1 (SORL1), complement component (3b/4b), clusterin and phosphatidylinositol- binding clathrin assembly protein have been reported. 17, 18 Environmental factors are of equal or greater importance in determining development of LOAD including antecedent head trauma, early hysterectomies, lower educational levels, cardiovascular disease and low levels of physical activity14. The neuropathological changes of AD commence in the third decade and a higher premorbid intellect correlates with protection from dementia in later life 19. Motor manifestations in LOAD are uncommon early in the course of the condition when the disease is confined to the temporal cortex. As the illness progresses, the earliest motor symptom is extrapyramidal rigidity, which if present early, implies another diagnosis or a poor prognosis3,4. Five to ten years into LOAD, patients may develop geggenhalten, apraxia and other frontal release phenomena as well as left hemibody neglect20. Myoclonus, seizures, and spasticity occur in the later terminal stages. Magnetic resonance imaging (MRI) of the brain reveals hippocampal and general cortical atrophy21. Brain proton emission tomography (PET) shows hypometabolism of the temporal and parietal lobes219. There are new techniques available to image amyloid plaque burden and distribution further assisting in confirming the antemortem diagnosis22. Treatment is directed at the cognitive symptoms and the psychiatric disturbances. Therapy of the cognitive disorder includes the use of cholinesterase inhibitors including donepezil, rivastigmine and galantamine in the early stages of the condition23. These treatments can be continued well into the disease as long as they are tolerated although data regarding efficacy of these agents after the first two to three years is inconsistent231. The NMDA receptor antagonist memantine reduces glutamate-mediated neurotoxicity of vulnerable neurons, and has Motor Sequela of Dementia, Devi 5 been approved for the treatment of moderate to severe AD24. Patients treated with a combination of a cholinesterase inhibitor and memantine fared better than those given either drug alone25. Atypical antipsychotic agents such as quetiapine are effective for associated psychotic symptoms and agitation and have fewer side effects, while serotonin reuptake agents are efficacious in treating depression in AD. Dementia due to Lewy Bodies: This is the second most common dementia accounting for 10 to 15% of cases at autopsy26. Subcortical and cortical Lewy bodies are associated with a variable combination of cognitive, psychiatric, and extrapyramidal features. Men are more affected than women with prevalence at autopsy of 1.5:1. The course was first considered to be far more rapid than AD with a survival of 2 to 5 years from presentation to death, but the current view is that for the majority of both DLB and AD patients, survival is about 12 years1,27. The clinical definition of DLB includes fluctuation of cognition and early prominence of psychiatric symptoms, especially visual hallucinations, in up to 75% of patients, and parkinsonian features that lead to frequent falls, rigidity, gait impairment; resting tremor infrequently occurs1,28. Symptoms of restless leg syndrome can precede the diagnosis of DLB by several decades and rapid-eye-movement sleep behavior disorder is a parasomnia frequently associated with DLB29. While a quarter of patients demonstrate rigidity and bradykinesia, the frequency varies depending upon patient selection bias and the confounding effects of neuroleptics. Postural instability, falls and syncope occur in up to a third of patients and should prompt consideration of DLB. Autonomic phenomena are more common in patients with DLB than in AD, particularly orthstatic hypotension and carotid-sinus hypersensitivity30. Urinary incontinence is an early phenomenon in DLB compared with AD31. Motor Sequela of Dementia, Devi 6 In contrast to AD, cortical Lewy bodies are preferentially deposited in the cingulate gyrus, insular cortex and temporal lobe with sparing of the hippocampus in cases of DLB, and neocortical neurofibrillary tangles are sparse or absent reflecting the difference in tau processing. Beta-amyloid protein levels are equally increased in both disorders. Patients with DLB and an excess of tangles demonstrate a clinical pattern more akin to AD, while those with fewer tangles present with the classical features of DLB1,32. Brain MRI of patients with DLB shows preservation of the volume of hippocampal and medial temporal lobes and SPECT demonstrates occipital hypoperfusion33. Electroencephalography may show slowing of the background and posterior dominant rhythms. Dopamine transporter loss in the caudate and putamen as demonstrated on fluoropropyl brain SPECT confers a diagnostic sensitivity of 83% and a specificity of 100%34. There are differences in the neuropsychological profile of DLB compared to AD. Patients with DLB perform quantitatively worse on learning and memory tasks when compared with AD patients of the same degree of dementia severity, and manifest differences in focal attentional ability on visual search tasks1,35. Treatment of the cognitive loss with cholinesterase inhibitors is associated with a consistently more robust
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